16,16-Dimethyl prostaglandin E2 reverses focal mucosal ischemia associated with stress ulcers

Harold V. Gaskill, Kenneth R Sirinek, Barry A. Levine

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Focal ischemia is postulated to contribute to gastric mucosal stress ulceration. This study evaluated directly (1) whether or not mucosal ulceration during hemorrhagic shock is preceded by focal gastric mucosal blood flow changes, and (2) whether or not topical Dm-PGE2 (16,16-dimethyl prostaglandin E2) affects focal gastric mucosal blood flow during hemorrhagic shock. Twelve anesthetized miniature swine had pyloric ligation and intragastric infusion of 5 ml/kg autogenous bile in 140 mM HCl. Gastric mucosal blood flow was documented by radiolabeled microspheres during (1) normotension, (2) initial hemorrhagic shock (50 mm Hg), and (3) hemorrhagic shock + 50 μg topical Dm-PGE2. Stable shock was then maintained for 3 hr. During this time ulceration developed, shedding radiolabeled microsphere-bearing mucosa into the lumen. Intact gastric mucosa and luminal contents were collected, weighed, and gamma counted. Blood flow to intact mucosa was calculated by standard techniques. The weight of shed tissue, as well as the blood flow to shed tissue, was calculated from luminal microspheres. Results: gastric mucosal blood flow was decreased 35% with hemorrhagic shock (28.8 ± 4.0 vs 18.7 ± 2.7 ml/100 g/min, P < 0.05). Blood flow to tissue which was subsequently shed averaged 6.4 ± 3.1 ml/100 g/min at the same time period (P < 0.05 vs surrounding tissue). Addition of Dm-PGE2 increased blood flow to shed tissue from 29 ± 8% to 48 ± 10% of blood flow to intact tissue (P < 0.05). Conclusions: (1) gastric mucosal ulceration is preceded by focal decreases in gastric mucosal blood flow, and (2) topical Dm-PGE2 reverses focal mucosal ischemia during hemorrhagic shock. Dm-PGE2's ability to reverse focal ischemia suggests a mechanism for prostaglandin-mediated cytoprotection.

Original languageEnglish (US)
Pages (from-to)83-88
Number of pages6
JournalJournal of Surgical Research
Volume37
Issue number1
DOIs
StatePublished - 1984

Fingerprint

Dinoprostone
Ulcer
Ischemia
Hemorrhagic Shock
Stomach
Microspheres
Mucous Membrane
Miniature Swine
Cytoprotection
Gastric Mucosa
Bile
Prostaglandins
Ligation
Shock
Weights and Measures

ASJC Scopus subject areas

  • Surgery

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16,16-Dimethyl prostaglandin E2 reverses focal mucosal ischemia associated with stress ulcers. / Gaskill, Harold V.; Sirinek, Kenneth R; Levine, Barry A.

In: Journal of Surgical Research, Vol. 37, No. 1, 1984, p. 83-88.

Research output: Contribution to journalArticle

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abstract = "Focal ischemia is postulated to contribute to gastric mucosal stress ulceration. This study evaluated directly (1) whether or not mucosal ulceration during hemorrhagic shock is preceded by focal gastric mucosal blood flow changes, and (2) whether or not topical Dm-PGE2 (16,16-dimethyl prostaglandin E2) affects focal gastric mucosal blood flow during hemorrhagic shock. Twelve anesthetized miniature swine had pyloric ligation and intragastric infusion of 5 ml/kg autogenous bile in 140 mM HCl. Gastric mucosal blood flow was documented by radiolabeled microspheres during (1) normotension, (2) initial hemorrhagic shock (50 mm Hg), and (3) hemorrhagic shock + 50 μg topical Dm-PGE2. Stable shock was then maintained for 3 hr. During this time ulceration developed, shedding radiolabeled microsphere-bearing mucosa into the lumen. Intact gastric mucosa and luminal contents were collected, weighed, and gamma counted. Blood flow to intact mucosa was calculated by standard techniques. The weight of shed tissue, as well as the blood flow to shed tissue, was calculated from luminal microspheres. Results: gastric mucosal blood flow was decreased 35{\%} with hemorrhagic shock (28.8 ± 4.0 vs 18.7 ± 2.7 ml/100 g/min, P < 0.05). Blood flow to tissue which was subsequently shed averaged 6.4 ± 3.1 ml/100 g/min at the same time period (P < 0.05 vs surrounding tissue). Addition of Dm-PGE2 increased blood flow to shed tissue from 29 ± 8{\%} to 48 ± 10{\%} of blood flow to intact tissue (P < 0.05). Conclusions: (1) gastric mucosal ulceration is preceded by focal decreases in gastric mucosal blood flow, and (2) topical Dm-PGE2 reverses focal mucosal ischemia during hemorrhagic shock. Dm-PGE2's ability to reverse focal ischemia suggests a mechanism for prostaglandin-mediated cytoprotection.",
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AB - Focal ischemia is postulated to contribute to gastric mucosal stress ulceration. This study evaluated directly (1) whether or not mucosal ulceration during hemorrhagic shock is preceded by focal gastric mucosal blood flow changes, and (2) whether or not topical Dm-PGE2 (16,16-dimethyl prostaglandin E2) affects focal gastric mucosal blood flow during hemorrhagic shock. Twelve anesthetized miniature swine had pyloric ligation and intragastric infusion of 5 ml/kg autogenous bile in 140 mM HCl. Gastric mucosal blood flow was documented by radiolabeled microspheres during (1) normotension, (2) initial hemorrhagic shock (50 mm Hg), and (3) hemorrhagic shock + 50 μg topical Dm-PGE2. Stable shock was then maintained for 3 hr. During this time ulceration developed, shedding radiolabeled microsphere-bearing mucosa into the lumen. Intact gastric mucosa and luminal contents were collected, weighed, and gamma counted. Blood flow to intact mucosa was calculated by standard techniques. The weight of shed tissue, as well as the blood flow to shed tissue, was calculated from luminal microspheres. Results: gastric mucosal blood flow was decreased 35% with hemorrhagic shock (28.8 ± 4.0 vs 18.7 ± 2.7 ml/100 g/min, P < 0.05). Blood flow to tissue which was subsequently shed averaged 6.4 ± 3.1 ml/100 g/min at the same time period (P < 0.05 vs surrounding tissue). Addition of Dm-PGE2 increased blood flow to shed tissue from 29 ± 8% to 48 ± 10% of blood flow to intact tissue (P < 0.05). Conclusions: (1) gastric mucosal ulceration is preceded by focal decreases in gastric mucosal blood flow, and (2) topical Dm-PGE2 reverses focal mucosal ischemia during hemorrhagic shock. Dm-PGE2's ability to reverse focal ischemia suggests a mechanism for prostaglandin-mediated cytoprotection.

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